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Overview of Petroleum Product Poisoning

By
Gary D. Osweiler, DVM, MS, PhD, Professor Emeritus, Veterinary Diagnostic and Production Animal Medicine, College of Veterinary Medicine, Iowa State University

Petroleum Product Poisoning

Overview of Petroleum Product Poisoning

Ingestion or inhalation of, or skin contact with, petroleum, petroleum condensate, gasoline, diesel fuel, kerosene, crude oil, or other hydrocarbon mixtures may cause illness and occasionally death in domestic and wild animals. Dogs and cats both may ingest petroleum products during grooming of contaminated fur or directly from open containers. Inhalation may occur in poorly ventilated areas where these chemicals have been used or stored. Ruminants may ingest such products in large amounts because they are thirsty, curious, or seeking salt or other nutrients, or if food or water is contaminated.

Small quantities of petroleum product used as carriers for insecticides have few or no harmful effects, but large quantities and prolonged exposure can induce severe reactions. Pipeline breaks, accidental release from storage, tank car accidents, and open or leaky containers are potential sources. Physical properties can affect exposure and toxicity. Volatility increases at lower molecular weight and lower saturation or aromaticity. Absorption is greater with highly volatile, lower molecular weight hydrocarbons (eg, hexane, gasoline) as well as aromatic hydrocarbons (benzene, toluene) because of greater lipid solubility. Crude petroleum that has lost much of its lighter, more volatile components through weathering may still be hazardous.

Crude oil and gasoline contain varying amounts of aromatic hydrocarbons, including benzene (2%–5% in gasoline), toluene, ethylbenzene, and xylene. These compounds ingested or inhaled in sufficient amounts can have acute and chronic effects different from those of other hydrocarbons that make up most oil and gas products. Benzene is hemotoxic and a known carcinogen at high levels of exposure. Toluene causes neurologic signs and damage at high dosages. Central nervous signs occur when sufficient petroleum product is absorbed into the brain or peripheral nerves. Toxicosis generally occurs rapidly after exposure.

Variation in composition of petroleum and petroleum-derived hydrocarbon mixtures explains some of the differences in toxic effects. Mixtures of low viscosity/high volatility (eg, gasoline, naphtha, kerosene, xylene) have a high aspiration hazard and irritant activity on pulmonary tissues. Gasoline and naphtha fractions may induce vomiting, which contributes to aspiration hazard. Fractions more viscous than kerosene (asphalt, mineral oil, waxes) are less likely to be inhaled and, even if aspirated, are somewhat less damaging to lung tissue. Older formulations of lubricating oils and greases can be particularly hazardous because of toxic additives or contaminants (eg, lead).

Clinical Findings:

Petroleum hydrocarbon toxicity may involve the respiratory, GI, or integumentary systems or the CNS. In most cases of ingestion, no clinical signs are seen, but small animals are reported to show oral irritation, salivation, and champing of jaws, followed by coughing, choking, and vomiting. Pneumonia due to aspiration of hydrocarbons into the lungs is usually the most serious consequence of ingestion of these materials. Aspiration can occur during vomiting by monogastrics or eructation of rumen contents. Pulmonary damage can occur from a combination of volatility, viscosity, and surface tension. Higher volatility promotes access of vapors to the lung and airways and displaces alveolar oxygen. Risk of pulmonary toxicity is increased by products of lower viscosity and surface tension, with increased penetration into smaller airways and spread of product to a larger lung surface area.

Acute bloat from petroleum products in ruminants has been reported after consumption of highly volatile hydrocarbons such as gasoline or naphtha. CNS signs may be a result of the anesthetic-like action of low-molecular-weight aliphatic hydrocarbons and/or cerebral anoxia that can result from lung damage or displacement of oxygen by the more volatile hydrocarbons. Some compounds when absorbed in high doses may sensitize the myocardium to endogenous catecholamines. Anorexia, decreased rumen motility, and mild depression may begin in ~24 hr and last 3–14 days depending on dose and content. Hypoglycemia may be seen several days after ingestion. These signs and weight loss may be the only responses seen in animals that do not bloat or aspirate oil. Some animals do not reestablish normal rumen function after ingestion and can develop a chronic wasting condition.

After ingestion of oil, the feces may not be affected until several days later, when they become dry and formed, in the case of kerosene or lighter hydrocarbon fractions; in contrast, heavier hydrocarbon mixtures (eg, motor oil) tend to be cathartic. Oil may be found in feces and rumen contents as long as 2 wk after ingestion. Regurgitated or vomited oil may be seen on the muzzle and lips.

CNS signs attributable to pulmonary, dermal, or GI absorption of hydrocarbons or cerebral anoxia include excitability (associated with aromatic fractions—benzene, toluene, etc), depression (aliphatic or saturated low-molecular-weight hydrocarbons), shivering, head tremors, visual dysfunction (sometimes associated with lead contamination), and incoordination. Acute pneumonia and possibly pleuritis (coughing, tachypnea, shallow respiration, reluctance to move, head held low, weakness, oily nasal discharge, and dehydrated appearance) are seen in some animals that aspirate highly volatile mixtures; deaths usually are seen within days. Respiratory signs may be limited to dyspnea shortly before death in animals that aspirate heavier hydrocarbons. Increased PCV, Hgb, and BUN, indicating mild to moderate hemoconcentration, are associated with development of pneumonia. Neutropenia, lymphopenia, and eosinopenia occur initially and are followed by a relative increase in neutrophils.

There are a few anecdotal reports of abortion after exposure. Laboratory data in rodents support the occurrence of increased fetal loss and decreased fetal growth. However, the doses necessary to affect the fetus were also sufficient to profoundly affect maternal health and weight.

Lesions:

Aspiration pneumonia is the most consistent postmortem finding in animals that do not die of bloat. This may be accompanied by tracheitis, pleuritis, and hydrothorax if highly volatile fractions such as gasoline or naphtha are involved. Lung lesions are usually bilateral and found in the caudoventral apical, cardiac, cranioventral diaphragmatic, and intermediate lobes. Affected portions are dark red and consolidated and may contain multiple abscesses. Encapsulated pulmonary abscesses may be found in cattle surviving up to several months after aspiration. Skin lesions may be obvious after repeated topical application or severe exposure and include drying, cracking, or blistering.

Diagnosis:

A hydrocarbon odor may be detected in lungs, ruminal contents, and feces. Even if ingested in large doses, hydrocarbons may not be visible in ruminal contents after ~4 days. Adding warm water to the GI contents may cause any oily contents to collect at the surface, but finding oil in the GI tract does not in itself justify a diagnosis of poisoning; most oils have low toxicity if not aspirated. Samples of GI contents, lung, liver, kidney, and the suspected source should be collected for chemical analysis to demonstrate presence of hydrocarbons in tissue (particularly lung) and GI contents and to match those found in tissues and ingesta with the suspected source. Samples must be carefully protected from cross-contamination during necropsy and transportation to the laboratory. Instructions from the receiving diagnostic laboratory should be checked to ensure collection equipment and transport containers are appropriate to prevent evaporative loss of important components and contamination. Positive chemical findings together with appropriate clinical and pathologic findings are confirmatory. Diagnosis in oil-field situations has historically been complicated by involvement of other toxicants, eg, explosives, lead from grease and “pipe dope,” arsenicals, organophosphate esters, caustics (acids or alkalis), and saltwater.

Treatment:

Bloat pressure should be released by passing a stomach tube if absolutely necessary to save the life of the animal; using a trocar risks forcing oil into the peritoneal cavity, which results in peritonitis. Passing a stomach tube dramatically increases the risk of aspiration, and extreme caution is necessary. In the absence of bloat, the prime objectives are to prevent aspiration and to mitigate GI dysfunction. Rumenotomy to remove ruminal contents and replace them with healthy ruminal material is safer. More chronic cases involving primarily hypofunction of the rumen may also respond to this procedure. Cathartics, if used, should be of the saline or sorbitol type; however, there is no evidence that they improve prognosis. Recent information no longer supports use of oil-based cathartics for petroleum ingestion.

Activated charcoal has occasionally been suggested for use in small animals. Although it does not effectively adsorb petroleum distillates, it may be given if necessary to adsorb additives and other contaminants. Gastric lavage is generally contraindicated for petroleum and volatile hydrocarbon ingestions. Care should be taken to avoid inducing vomiting and aspiration. Small animals with acute respiratory distress may require supplemental oxygen and positive-pressure ventilation, used cautiously because of existing physical pulmonary damage. Frequent purging of ventilators is necessary to eliminate volatile hydrocarbons.

Animals with evidence of bacterial respiratory infection may require broad-spectrum antibiotic treatment. Pathogens can be introduced into the lungs from aspirated rumen or stomach contents mixed with the hydrocarbons. However, the use of steroids in hydrocarbon aspiration may further reduce the chance of recovery and are generally contraindicated. Treatment of aspiration pneumonia (see Aspiration Pneumonia) is rarely effective, and the prognosis is poor. However, because signs of aspiration may not appear for several days, prognosis based on initial clinical findings may be misleading.

Most high-molecular-weight compounds pass through the GI tract unchanged. Most of the petroleum hydrocarbons are highly lipophilic and will be stored for varying times in tissues with high lipid content, including fat, nervous tissue, and the liver. Some of the absorbed compounds are metabolized into more toxic by-products (eg, benzene, toluene, and n-hexane). Although most of these compounds do not remain in the body for prolonged periods, little is known about exactly how long tissue levels persist in highly exposed animals. The potential for tissue residues must be considered before the slaughter of animals intended for human consumption.

In poisoning or damage due to cutaneous exposure, the material should be removed from the skin with the aid of soap or mild detergents and copious amounts of cool water. The skin should not be brushed or abraded. Further treatment depends on the clinical signs and is largely restricted to supportive therapy.

Petroleum hydrocarbon poisoning can be avoided only by preventing access to these materials through proper storage of home and farm chemicals and well-maintained fencing around high-risk petroleum facilities.

Effects of Oil and Gas Fields on Cattle Health and Production:

Anecdotal reports in the literature have documented producer concerns about the effect of oil fields on cattle health and production. Some observational studies have suggested that exposure to emissions from sour gas processing plants and sour gas flares (natural gas containing hydrogen sulfide) may be associated with an increased risk of certain reproductive losses in cattle. Researchers are currently reexamining these findings and exploring the impact of oil and gas field emissions on the immune system.

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